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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Minnesota strain of turkey enteric coronavirus (TCV) was grown on a human rectal tumor (HRT-18) cell line in the presence of radiolabeled amino acids and glucosamine to analyse virion structural proteins. In addition to the 52,000 unglycosylated nucleocapsid protein, three major glycoprotein species were found to be associated with the viral envelope. A predominant glycosylated protein with a molecular weight of 22-24,000 represented the transmembrane matrix protein. Larger glycoproteins with apparent molecular weights of 180-200,000 (gp 200), 120-125,000 (gp 120) and 95-100,000 (gp 100) were associated to the characteristic large bulbous projections (peplomers) located at the surface of the virion. The gp 100 and gp 120 species apparently arose from a proteolytic cleavage of gp 200, as suggested by digestion studies with trypsin and chymotrypsin. An additional large glycoprotein with mol. wt. of 140,000 (gp 140), that behaved as a disulfide-linked dimer of a 66,000 molecule, was found to be associated to granular projections located near the base of the large peplomers. Digestion studies with trypsin, bromelain and pronase demonstrated that gp 140 was related to the hemagglutinating activity of the virus. An inner membranous sac or tongue-shaped structure could be visualized in the interior of the viral particles following treatment with pronase. In contrast, trypsin or chymotrypsin treatments resulted in evaginations ("budding") on the virus surface. Progeny viral particles produced in TCV-infected cell cultures in the presence of tunicamycin lacked both types of surface projections, as demonstrated by electron microscopy and electrophoresis. The matrix protein also appeared to be reduced to its unglycosylated form, concomitant with a considerable loss of its antigenicity. Thus, with respect to its morphological and biochemical characteristics, TCV resembles viruses belonging to the group of mammalian hemagglutinating coronaviruses, but differs in that both types of envelope glycoproteins are N-glycosylated as in case of the avian infectious bronchitis virus.
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PMID:Identification and location of the structural glycoproteins of a tissue culture-adapted turkey enteric coronavirus. 267 55

Granules that are potently cytolytic in vitro can be obtained from cytotoxic lymphocytes that kill virally infected cells and tumor cells. These granules contain pore-forming proteins and several serine proteases. Here we indicate that at least two different proteases participate in the lysis mediated by granule proteins from RNK-16 rat leukemia cells. We report twelve different mechanism-based or "suicide" isocoumarin serine protease inhibitors which have different 3- and 7-substituents that confer selectivity and reactivity towards either the chymotrypsin- ("chymase") or trypsin-like ("tryptase") protease activities of RNK-16 cells. Second order inhibition rates of inactivation (kobsd/[I]) for the RNK-16 granule proteases ranged between 164 and 22,640 M-1s-1. These new, specific and highly reactive isocoumarin serine protease inhibitors also abrogated the cytolysis mediated by lymphocytes granule proteins. The eight inhibitors with large hydrophobic or basic substituents that conferred chymase or tryptase specificities were more effective at inactivating lytic function than the four elastase-directed inhibitors with smaller substituents. All twelve new isocoumarin inhibitors blocked cytolysis at lower concentrations than 3,4-dichloroisocoumarin, a potent general mechanism-based serine protease inhibitor that also blocks RNK-16 granule protease activities and lysis.
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PMID:Selective isocoumarin serine protease inhibitors block RNK-16 lymphocyte granule-mediated cytolysis. 281 73

The immunoperoxidase avidin-biotin-peroxidase complex method was used to investigate the presence of histiocyte markers such as lysozyme, alpha-1-antitrypsin (A1AT) and alpha-1-anti-chymotrypsin (A1ACT) and of vimentin, a specific marker for mesenchymal differentiation, in a spontaneous and transplantable rat tumor of supposed fibroblastic-histiocytic origin. Positive staining was obtained for lysozyme and vimentin but A1AT and A1ACT were not demonstrable in any of the tumor sections. These results provide evidence for the fibro-histiocytic nature of the tumor studied and suggest its classification as a malignant fibrous histiocytoma (MFH).
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PMID:Immunohistochemical identification of lysozyme and vimentin in an experimental malignant fibrous histiocytoma. 285 48

When tumor cells develop in healthy adults, they activate the cellular immune system--natural killer (NK) cells, antigen-specific cytotoxic lymphocytes (CTL), and the synthesis of antigen specific cytotoxic antibodies. These are aimed at killing the intruding cells. However, in cancer patients the tumor continues to grow. As tumor cells proliferate, they were shown to release factors that mediate the inactivation of the host immune defense systems. The study documented in this article examined peripheral blood lymphocytes, mononuclear cells (MNC), NK cells, T-helper cells (THC). This study confirmed the interaction of the released inhibitor factors with these mononuclear cells. NULL cells from healthy adults responding to interleukin-2 (IL-2) and NILL cells from patients with metastatic breast carcinoma nonresponsive to IL-2 were also isolated by the standard antibodies-pinning technique. The cells were obtained from age-matched subjects: ten healthy adults; ten patients each from Stage I, II, III, and IV metastatic breast carcinoma (BCa-I, BCa-II, BCa-III, and BCa-IV or MBCa); and ten patients with benign breast disease (BBD). The responsiveness of these THC, PBMNC, NK, NULL, and NILL cells in vitro to graded levels of phytohemagglutinin (PHA), Concanavalin A (Con A), and recombinant interleukin-2 (rIL-2) was examined. Responsiveness was monitored by 3H-thymidine (3H-TdR) uptake, production and release of IL-2, interleukin-2 receptor (IL-2R), and cytotoxic activities against K-562 cells and breast carcinoma short-term cell lines. A lack of functional IL-2R in peripheral blood lymphocytes from patients with metastatic breast carcinoma was confirmed by nonsignificant anti-Tac antibody binding. An elevation in the expression of cell surface antigen GP-120 has been observed to be associated with the activation in vitro of T-cells from healthy adults and from patients with benign breast disease, but not of T-cells from patients with breast carcinoma. Biochemical studies of the GP-120 using high performance liquid chromatography combined with nitrocellulose blotting confirmed that the glycoprotein was resistant to trypsin and chymotrypsin, but susceptible to pronase. It contained sialic acid and lactosaminoglycan as O-linked sugars. It could be labeled with pariodate/NaB(3H4) and is recognized by MAbT-305 monoclonal antibodies. It contained sialic acid linked (2---3) to galactose.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Peripheral blood lymphocytes from patients with cancer lack interleukin-2 receptors. 296 32

An antiproliferative suppressor lymphokine was produced from rat T-cells specifically in response to the poorly immunogenic syngeneic mammary adenocarcinoma 13762A. The tumor-induced suppressor lymphokine (TISL) was produced late in culture (peak production on Days 4 and 5) and showed strong but selective inhibitory activity on a variety of immune responses. The immune peritoneal exudate cell response to a highly immunogenic clone from the parental tumor (clone 18A) and the concanavalin A-stimulated response of nonimmune spleen cells were inhibited strongly by TISL. In contrast, the immune spleen cell response to 13762A and the lipopolysaccharide response of nonimmume spleen cells were unaffected. Preliminary molecular weight and physicochemical analysis of TISL indicated that the molecule was large (Mr greater than 350,000); partially sensitive to 75 degrees C treatment for 15 min and to pH 2.0 treatment; only partly degraded by the enzymes trypsin, chymotrypsin, and proteinase K; and completely destroyed by boiling. Although TISL was produced specifically in response to 13762A tumor, prior immunization in vivo was not necessary for the induction of the suppressor lymphokine. These results indicate that populations of rat lymphocytes contain naturally occurring TISL secreting cells, which can be activated specifically by tumor antigens such as those expressed by 13762A.
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PMID:Suppressor lymphokine produced by rat T-cells in response to syngeneic mammary adenocarcinoma 13762A. 296 35

The killing of human glioma by lymphokine activated killer (LAK) cells was studied. LAK cells generated by culturing recombinant interleukin-2 (IL-2) with human peripheral blood lymphocytes (PBL) obtained from normal volunteers markedly lysed allogeneic glioma grown in tissue culture. Susceptibility of glioma to lysis by LAK cells was abrogated by pretreating the glioma cells with trypsin or chymotrypsin, but was unaffected by pretreatment with hydrocortisone, neuraminidase, glycosidases or sodium periodate. These results suggest that the cell surface determinant on human glioma cells responsible for its tumor selective lysis by LAK is a protein sensitive to trypsin and chymotrypsin.
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PMID:Lymphokine activated killer (LAK) cell mediated killing of human glioma: effect of pretreating glioma with various membrane modifying agents. 303 36

Recently, we reported a lymphokine, monocyte cytotoxicity-inducing factor (MCF), which is distinct from interferon-gamma (IFN-gamma). In this report, we provide further characterization of MCF. MCF is inactivated by chymotrypsin, but not trypsin, RNase, or DNase. The production of MCF is abolished in a dose-dependent manner by actinomycin D and is diminished by puromycin, and cycloheximide. Native MCF produced under serum-free conditions demonstrated charge heterogeneity with three species having isoelectric points at 2.7, 5.6, and 6.7 respectively, and two molecular weight species of 29 Kd and 14.7 Kd. MCF-activated monocytes were not only able to lyse both NK sensitive and resistant targets, but also secreted IL 1, but not TNF. In summary, MCF is a lymphokine distinct from TNF, IL 1, IL 2, the IFNs, and the CSFs, which is able to activate monocytes to lyse tumor targets.
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PMID:Characterization of a human monocyte cytotoxicity-inducing factor (MCF). 306 22

Treatment of the rat pancreatic acinar cell line AR4-2J with the calcium ionophore A23187 selectively increases, within a few hours, the steady-state level of trypsin mRNA. Addition of the tumor-promoting phorbol ester phorbol 12-myristate 13-acetate potentiates the calcium-induced increase. The mRNA level of the other tested exocrine pancreatic genes decreases. These results were confirmed by DNA transfection experiments, using the 5' flanking region of the trypsin and chymotrypsin genes linked to the coding sequence of the chloramphenicol acetyltransferase (CAT) gene. In calcium-induced cells transfected with the trypsin constructs, an increase in CAT activity was observed, whereas the chymotrypsin constructs revealed a decreased CAT activity. Glucose starvation of AR4-2J cells similarly elicited a selective increase in trypsin mRNA. This selective regulation of trypsin may reflect its role as the key activator of the other zymogen species.
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PMID:Selective regulation of trypsin gene expression by calcium and by glucose starvation in a rat exocrine pancreas cell line. 308 79

Monoclonal antibodies (MAbs) were generated by immunizing mice with the mesothelioma cell line SPC111 and selected by indirect immunofluorescence on viable cells. Indirect immunofluorescence staining and radioimmunoassays demonstrated selective binding of the antibodies ME1 and ME2 with the surface membrane of mesothelioma, but not with lung adenocarcinoma cell lines. Lung small-cell carcinoma cell lines were unreactive, while staining was seen in a proportion of lung squamous-cell carcinoma cell lines. The antibodies were unreactive with other cell lines, including breast, colon, ovarian, and renal-cell carcinoma, leukemia, and lung fibroblast. The antibodies stained normal mesothelial cells, but were unreactive with normal bronchial epithelial cells in primary cultures, or peripheral blood cells. Immunohistochemical staining of cryostat sections of tumor tissues confirmed the ability of the antibodies to distinguish between mesothelioma and lung adenocarcinoma. All 12 mesothelioma tissues, but none of 9 lung adenocarcinomas or large-cell carcinomas, stained with the MAbs. Staining of malignant mesothelioma tissues was very homogeneous. Some lung squamous-cell carcinomas and breast carcinomas were stained focally by both, and some ovarian carcinomas by one antibody. Solid-phase radioimmunoassays demonstrated antigen sensitivity to chymotrypsin digestion and binding competition between the antibodies. The antibodies ME1 and ME2 identify a surface membrane antigen with preferential expression on normal and malignant mesothelial cells. They distinguish malignant mesothelioma from lung adenocarcinoma on cryostat sections and promise to be useful tools in biological studies of mesothelial cells.
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PMID:Monoclonal antibodies against mesothelial membrane antigen discriminate between malignant mesothelioma and lung adenocarcinoma. 327 35

The killing of Fischer rat 9L glioma in vitro by lymphokine-activated killer (LAK) cells was studied. LAK cells generated by culturing Fischer spleen cells with recombinant interleukin 2 markedly lysed glioma cells but did not kill syngeneic normal brain tissue in a chromium release microcytotoxicity assay. Susceptibility of glioma to lysis by LAK cells was markedly diminished by pretreating the glioma cells with trypsin or chymotrypsin but was unaffected by pretreatment with neuraminidase, glycosidases, or sodium periodate. These results suggest that LAK cell killing of glioma is probably tumor-selective and that a crucial cell surface determinant on glioma cells responsible for its tumor-selective lysis by LAK is a protein sensitive to trypsin and chymotrypsin.
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PMID:Lymphokine activated killer (LAK) cell-mediated lysis of murine glioma: trypsin-chymotrypsin-sensitive glioma protein is responsible for tumor-selective recognition by LAK cells. 348 96


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